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Toxicology Flashcards

1
Q

What is enterohepatic recirculation?

A

Occurs when a toxin is excreted form the liver, via bile, which is then deposited in SI where it can be reabsorbed, sometimes repeatedly, extending its toxic effects

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2
Q

What is P glycoprotein?

A

A drug transporter on the luminal surface of brain capillaries, responsible for transport of substances from the brain tissue back into capillary lumen, limiting brain exposure to drugs and toxins

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3
Q

What population may have an undeveloped BBB?

A

Young animals

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4
Q

How does MDR1 play into the BBB?

A
  • MRD1 controls P glycoprotein
  • Certain breeds of dogs lack full expression of the gene and are susceptible to toxic brain exposure to drugs at normal therapeutic doses
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5
Q

Dermal decontamination of a patient should be done with (dishwashing/dishwasher) soap

A

Dishwashing

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6
Q

What type of substances can be readily absorbed via the dermis?

A

Lipophilic substances

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7
Q

Why are alkaline agents more destructive to the eye?

A

They cause a liquefactive necrosis which results in transformation of tissue into a liquid viscous mass that can damage deeper layers

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8
Q

Why do acidic agents not cause as much damage as alkaline agents (to the eye)?

A

They do not penetrate tissues as well and self limit due to precipitation of epithelial proteins

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9
Q

How should of ingestion of corrosive substances be treated?

A
  • Rapid dilution with water or milk
  • Emesis CONTRAINDICATED because it can re-expose the oral tissues to the caustic agent, leading to significant damage
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10
Q

In what species is emesis contraindicated?

A
  • Rabbits and rodents
  • Weak stomachs and lack the natural ability to vomit?
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11
Q

Why is syrup of ipecac no longer recommended as an emetic agent?

A

Carries a risk of cardiotoxicity, HGE, skeletal muscle weakness

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12
Q

Why is hydrogen peroxide not recommended as an emetic agent in cats?

A

Can cause refractory vomiting

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13
Q

How does apomorphine exert its effect?

A

It is a dopaminergic agonist - its stimulates dopamine receptors in the CRTZ which activates the VC

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14
Q

What drug can be used to treat the sedation caused by apomorphine?

A

Naloxone - it will reverse the sedation but not the emesis

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15
Q

When is gastric lavage most effective?

A

<4 hours post ingestion

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16
Q

What substances does AC not bind to?

A
  • Strong acids/alkalis
  • Alcohols (ethanol/methanol)
  • Cyanide
  • Lithium
  • Ethylene glycol
  • Metal (iron)
  • Bleach
  • Xylitol
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17
Q

Why do electrolytes need to be monitored with giving multiple doses of AC?

A

It has strong osmotic properties that can create serious imbalances

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18
Q

What is cholestyramine?

A
  • Bile acid sequestrant
  • Binds bile in the GIT to prevent its reabsorption
  • Strong ion exchange resin –> exchanges Cl anions with anionic bile acids in GIT and binds them strongly in resin matrix for elimination
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19
Q

What is ion trapping?

A
  • It increases the excretion rate of toxic drugs
  • Most drugs are weak acids or weak bases
  • Drugs typically are unable to pass through cell membranes unless they are in a non ionized state
  • Weak acid drugs are absorbed best when placed in an acidic environment as they will be in a non ionized stated
  • Weak base drugs are absorbed best when placed in an alkaline env
  • By modifying pH of a surrounding env, we can modify ionization trap a drug, and prevent its absorption
  • Technique used for drugs that are readily absorbed in kidney’s nephron or bladder
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20
Q

What is the lipid sink theory?

A
  • Provides a “sink” where fat soluble toxins can be bound and excreted without being metabolized
  • ILE expands intravascular lipid phase which sequesters lipophilic toxins within it, reducing effect site concentration and toxicity until compound is metaboilized and excreted
  • Sink is not selective and will also absorb therapeutic drugs
  • Permethrins, baclofen, some antidepressants, bupivicaine, moxidectin, NSAIDs, Ca channel blockers, beta blockers, avermectins, cannabis, amphetamines,
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21
Q

What is NAPQI?

A
  • A highly reactive toxic metabolite
  • Causes severe oxidative damage to RBC by causing oxidation of Hb to metHb, which does not carry oxygen
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22
Q

What is the toxic dose of acetaminophen for cats?

A

10mg/kg

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23
Q

What is the toxic dose of acetaminophen for dogs?

A

75mg/kg

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24
Q

What eye condition can be seen in toxic of acetaminophen?

A

KCS

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25
Q

How does acetaminophen cause toxicity?

A
  • Metabolized by the liver via sulfation & glucoronidation
  • Major pathway converts acetaminophen to inactivate metabolites through conjugation to inactive glucuronide and sulfate metabolites
  • Minor pathway metabolizes a/m by the P450 mixed function oxidase to NAPQI
  • In normal circumstances, this minor route produces little NAPQI, but in toxicity, the glucuronidation pathway becomes saturated
  • In normal circumstances, glutathione detoxifies NAPQI, but in toxicity, glutathione stores quickly become depleted, leaving NAPQI free to bind to lipids in the hepatocyte membrane and causing hepatocellular necrosis
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26
Q

How does NAC act as an antidote for a/m toxicity?

A
  • Provides a substrate for glutathione, allowing inactivation of toxic metabolites
  • Repeated doses due to enterohepatic recirculation
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27
Q

Why are CYP 450 inhibitors contraindicated as treatment for acetaminophen toxicity in cats?

A

Cats utilize the CYP pathway to convert methemoglobin to Hb

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28
Q

What are some treatments for acetaminophen toxicity?

A
  • NAC
  • Cytochrome P450 inhibitors (cimetidine, ranitidine - slow metabolism of acetaminophen)
  • Ascorbic acid (used for methemoglobinemia in affected cats
  • Feed cats kitten food due to increased sulfhydryl group substrates
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29
Q

How can most adhesives be removed?

A

With vegetable oil, which can then be washed off with dishwashing soap

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30
Q

What is the toxic component of alliums?

A
  • Propyl disulfide
  • Metabolism produces oxygen free radicals
  • Erythrocytes are sensitive to oxidative injury
  • Disulfides denature Hb, which forms Heinz bodies, which are then removed from circulation via hemolysis
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31
Q

In what form are alliums toxic?

A
  • All toxic regardless of whether it is raw, cooked, or dehydrated
  • Dehydrated will cause signs at lower doses than raw
  • Cats fed baby food with as little as 0.3% onion powder can become affected
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32
Q

What is amitraz?

A
  • An alpha 1 & 2 adrenergic agonist applied topically to control ticks, mites, lice. Affects a1 & a2 adrenergic receptors in CV system
  • Cats are highly sensitive to its effects
  • Hyperglycemia common
  • Avoid atropine even in face of bradycardia - likely to produce significant tachycardia
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33
Q

Are ant traps toxic?

A

Some contain arsenic but have low concentrations of toxins and are a very small size - likely no problem of toxicity, risk of FB is higher

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34
Q

How do anticoagulant rodenticides work?

A
  • By antagonizing Vit K epoxide reductase, preventing the activation of clotting factors II, VII, IX, X. Depletion of these factors slows all coagulation pathways
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35
Q

Why is PT the first to show an issue?

A

F VII only has a half life of 6 hours

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36
Q

How long do 1st generation rodenticides depress clotting factors?

A

7-10 days, -farins

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37
Q

How long do 2nd generation rodenticides depress clotting factors?

A

3-4 weeks, - coums

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38
Q

Enterohepatic recirculation can occur with which anticoagulant rodenticide?

A

Brodifacoum

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39
Q

How long will it take for Vit K to start restoring new clotting factors?

A

12-24 hours

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40
Q

What are the 4 main groups of antidepressants?

A
  • MAOI inhibitors
  • Tricyclics
  • SSRIs
  • Atypical
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41
Q

How do MAOIs work?

A
  • Monoamine oxidase is an enzyme that breaks down norepi, epi, dopamine, and serotonin
  • When enzyme is inhibited, the levels of these neurotransmitters increase
  • Hypo or hypertension, CNS depression, arrythmias, coma, death
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42
Q

How do tricyclics work?

A
  • Block reuptake of norepi and serotonin, increasing their levels
  • Produces similar signs as MAOI
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43
Q

How do atypicals work?

A
  • Cause levels of serotonin, norepi, and dopamine to increase
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44
Q

What is serotonin syndrome?

A
  • Results from excess serotonergic antagonism of serotonin receptors in the CNS & PNS
  • Causes mental status changes, neuromuscular abnormalities and autonomic instability
  • Patients present lethargy, which progresses to agitation
  • Thermoregulatory center frequent reset - present hyperthermic
  • Tremors, seizues
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45
Q

What is the treatment for serotonin syndrome?

A
  • Emesis
  • AC
  • Phenothiazines are serotonin antagonists
  • Cyproheptadine is a nonspecific serotonin antagonist
  • Propranolol is a serotonin receptor antagonist
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46
Q

What drugs can cause serotonin syndrome?

A
  • Amantadine
  • Bupropion
  • Carbamazepine
  • Codeine
  • Tramadol
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47
Q

What is the toxic component of autumn crocus and how does it exert its effect?

A
  • Colchicines and other alkaloids
  • Toxin arrests mitosis, leading to apoptosis/cell death
  • Particular threat to felines
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48
Q

Which toxicity can cause a flaccid paralysis?

A

Avermectins

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49
Q

How do avermectins exert their effect?

A
  • GABA agonism; hyperpolarizes cell membranes and prevents neuronal depolarization, leading to flaccid paralysis
  • MRD1 dogs can show toxicity at lwoer levels
  • Works by inhibiting Cl channels
  • In vertebrates at high enough doses, can overwhelm the BBB and enter CNS
  • Toxicity often occurs from dogs receiving LA doses, or eating feces of LA
  • Often combined with spinosad, an antiparasitic, which lowers the toxicity threshold for ivermectin by permitting more to remain in the CNS
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50
Q

What are the toxic doses for avermectins?

A
  • Dogs: 2.5mg/kg
  • Cats: 1.3mg/kg
  • Sensitive dogs: 100-500mcg/kg
  • Young dogs: 300mcg/kg
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51
Q

What is the treatment for avermectin toxicity?

A
  • Decontamination and supportive care
  • Undergoes enterohepatic recirculation
  • Lipid soluble toxin
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52
Q

Should emesis be performed in cases of ingestion of bleach and household cleaners?

A

No

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53
Q

What is bromethalin and how does it exert its effect?

A
  • A non anticoagulant rodenticide made to kill warfarin resistant rats
  • Works by uncoupling of oxidative phosphorylation in the CNS & liver mitochondria
  • This causes a decrease in ATP production and then causes ATP dependent transport pumps to not function
  • This results in the loss of ability to maintain osmotic gradient and membrane potential into cell
  • This leads to a build up of intracellular Na that causes water to move into cells and they swell with water
  • Na influx into brain cells causes cerebral edema and loss of function
  • CNS signs occur from increased ICP due to fluid shift
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54
Q

What are bromethalin toxicity signs classified as?

A
  • Paralytic or convulsant (dose dependent)
  • Paralytic = amount ingested greater than lethal dose but less than LD50
  • Convulsant = amount ingested is greater than LD50
  • Final stages of toxicity may be decerebrate posture
  • Cats paralytic regardless of dose
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55
Q

How many cannabinoid receptors do dogs and humans have?

A

2, CB1 (primarily in CNS and responsible for most clinical effects), and CB2 (peripheral tissues)

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56
Q

Does THC undergo enterohepatic recirculation?

A

Yes, and has a long half life due to lipid solubility

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57
Q

Carbamates

A
  • Found in dusts, shampoos, flea and tick collars
  • Cause nearly identical toxicity to organophosphates, except that it is a REVERSIBLE inhibition of cholinesterase activity
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58
Q

What plants are cardiac glycosides?

A

Kalanchoe spp
- Foxglove
- Lily of the valley
- Oleander
- Laurel
- Dogbane
- Some milkweeds

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59
Q

How do cardiac glycoside plants exert their effects?

A
  • Inhibit sodium/potassium ATPase
  • K accumulates outside cell, preventing Ca release
  • Intracellular Na increases and K levels decrease
  • Increased Na can be exchanged for Ca, which improves contractility and is how digoxin works as a positive inotrope
  • Very small therapeutic window, with too much, there is a progressive decrease of electrical conductivity
  • This causes frequent and irregular depolarization of cells
  • Result is disorganized cardiac electrical activity, manifesting in cardiac arrhythmias and possible arrest
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60
Q

Do cardiac glycosides undergo enterohepatic recirculation?

A

Yes

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61
Q

Where is the highest concentration of the cardiac glycoside toxin found?

A

In the flower, but the water is also toxic

62
Q

The castor bean contains what toxin?

A

Ricin

63
Q

Factors about the castor bean

A
  • Toxic in all parts of the plant, but most concentrated in the bean
  • Bean coat must be broken to release ricin, therefore ingestion of the entire bean = little absorption
  • Toxin is destroyed by moist heat, so castor oil is NOT toxic if it has been extracted correctly
64
Q

MOA of ricin

A
  • Disturbs calcium homeostasis by decreasing calcium uptake, result in an increased sodium/calcium exchange and disturbance of cardiac nerve conduction
  • Clinical signs usually occur within 6 hours of ingestion
  • Damage to GIT, may see hepatic failure
65
Q

What is cholecalciferol?

A

Active Vit D3 - promotes body’s retention of Ca

66
Q

MOA of cholecalciferol

A
  • Ca reabsorption from bone and intestine into blood, then increased Ca absorption by kidneys occurs
  • HyperCa and tissue mineralization leads to renal tubular injury
  • Death occurs from hypercalcemic cardiotoxicity
  • Cats more sensitive to toxicosis
67
Q

What are some treatments for cholecalciferol toxicity?

A
  • Emesis, AC, IVFT (NOT lrs - contains Ca)
  • ILE (highly lipophilic)
  • Furosemide (increases Ca excretion from kidneys)
  • Prednisone (decreases Ca reabsorption rom bones and intestines)
  • Calcitonin (induces calciuresis and reduces resorption of Ca from bone)
  • Pamidronate disodium (inhibits osetoclastic bone resorption)
  • Clodronate (biphosphonate)
68
Q

MOA of cyanide

A
  • Inhibits cellular respiration and displaces oxygen from Hb molecule by converting Hb to cyanohemoglobin, which cannot carry O2
  • Detox occurs via hepatic metabolism, which is easily overwhelmed
69
Q

At what dose of sodium nitroprusside can cyanide toxicity be seen?

A

> 2mcg/kg/min

70
Q

What are the antidotes to cyanide toxicity?

A
  • Sodium nitrate, sodium thiosulfate, and hydroxycobalamin
  • Oxygen
71
Q

What bitter flavor has been added to all antifreezes in the US?

A

Denatonium benzoate

72
Q

What are the lethal doses of ethylene glycol toxicity?

A
  • Dogs: 4.4ml/kg
  • Cats: 0.9ml/kg due to higher baseline production of oxalic acid
73
Q

Where does metabolism of ethylene glycol occur?

A
  • Primarily in liver
  • Alcohol dehydrogenase converts EG to glycoaldehyde –> glycolic acid –> glycoxylate/glycoxylic acid –> oxalic acid
  • Oxalic acid forms insoluble calcium oxalate crystals, which precipitate in renal tubules, resulting in ARF
74
Q

What happens in stage 1 of EG toxicity?

A
  • Neurologic stage
  • CNS depression, ataxia
  • Appear intoxicated
  • As serum osmolality increases, PU/PD nay occur - transient
  • Pet appears to recover
  • Cats may have elevation of 3rd eyelids
  • Can last up to 12 hours post ingestion
75
Q

What happens in stage 2 of EG toxicity?

A
  • Acidotic phase
  • Effects are due to an increase in the acidic metabolites
  • 12-24 hours post ingestion
  • Cardiorespiratory effects (tachycardia, tachypnea)
  • High AG (40-50mEq/L)
  • Hypocalcemia (bc it is binding with oxalic acid)
  • Hyperglycemia
  • Increased renal enzymes, hyperK
76
Q

What happens in stage 3 of EG toxicity?

A
  • 24-72 hours post
  • Oral ulceration, anuria, oxalate crystals in urine
  • Indicated by renal failure
  • Azotemia –> isosthenuria –> oliguria
77
Q

What is seen on UA in EG patients?

A
  • Glucosuria
  • Renal tubular casts
  • Isosthenuria
  • CaOx crystals (usually monohydrates)
78
Q

What may be seen on AFAST in EG patients?

A
  • “Halo sign” of kidneys
79
Q

What are the antidotes to EG?

A
  • Ethanol = competes for the active site of alcohol dehydrogenase. A/D has a much higher affinity for ethanol than EG. CRI of 7% ethanol. Exacerbates osmotic diuresis and increases plasma osmolality
  • Fomepizole (4MP) = A more specific and effective alcohol dehydrogenase inhibitor that directly competes with EG and prevents EG metabolism and allows it to be excreted unchanged. Do not administer concurrently with ethanol as fatal alcohol toxicosis will occur
  • AC not very helpful, absorbs very little
80
Q

What occurs with garbage ingestion?

A
  • Enterotoxemia
  • Small bowel pH may increase >6, which results in absence of HCl acid. HCl prevents multiplication of acid, and achlorhydria increases risk of enterotoxemia
  • Streptococcus, Salmonella, Bacillus
81
Q

Glow jewelry

A
  • Toxic compound is dibutyl phthalate, which is what lends luminescence
  • Low toxicity
82
Q

Grapes and raisins

A
  • Toxic principle unknown
  • May also be caused by currents
  • Both white and red grapes
  • Proximal renal tubular necrosis has been documented on histo
83
Q

Lead

A
  • Results in nervous tissue demyelination, and interference with GABA, cholinergic function, and heme synthesis
84
Q

What bloodwork changes are seen on CBC?

A
  • Large # of nRBC
  • Anemia
  • Basophilic stipling
85
Q

How do you treat lead toxicity?

A
  • Lead must be removed
  • AC not helpful
  • Treat with a chelating agent: Ca EDTA. May cause renal tox
  • D-penicillamine
  • Dimercaptosuccinic acid
  • Dimercaprol
  • Succimer
86
Q

What are the toxic lily species?

A
  • Lilium & Hemerocallis
  • Easter lilies, stargazer, asiatic, oriental, tiger, rubrum, Japanese snow, various day lilies
87
Q

Which lilies are not true lilies?

A
  • Peace lily
  • Lily of the valley
88
Q

Which parts of the lily plant are toxic?

A

The entire plant

89
Q

Are dogs affected by lily toxicity?

A

Dogs will experience GIT signs without renal failure

90
Q

What happens in lily toxicosis in cats?

A
  • Causes acute nephrotoxicity
  • Proximal convoluted tubular necrosis occurs
  • Necrosis appears to occur in renal tubular epithelial cells but not in basement membrane, so aggressive tx can help as these cells can regenerate
  • Crea is often elevated disproportionally to BUN conc
  • Kidneys are often swollen and may have perirenal edema
91
Q

What does macadamia nut ingestion cause?

A
  • Tremors, weakness, agitation, v/d, paralysis (primarily rear limbs)
  • Clinical signs w/i 12 hours of ingestion: 2.4-62.4g/kg
  • MOA unknown
92
Q

What is metaldehyde?

A

A highly palatable snail/slug killer

93
Q

How does metaldehyde cause toxicity?

A
  • MOA unknown
  • Theory is conversion to acetaldehyde in stomach when exposed to acidic environment decreases brain GABA, serotonin, and norepi. The decreased concentration of inhibitory neurotransmitters results in convulsions
  • As toxicity progresses, CNS stimulation becomes CNS depression
  • Liver injury may occur days after
  • AC can be used, however it is poorly lipophilic, ILE not a good option
94
Q

Methylxanthine toxicity

A
  • Adenosine receptor antagonist in CNS
  • Direct myocardial stimulator
  • Toxicity causes adenosine receptor blockage and increases in cyclic adenosine monophosphate, results in increased Ca conc within cell which leads to increased muscular contractility and CNS stimulation
  • Rapidly absorbed in mouth; can be reabsorbed from bladder and perpetuate toxicity
  • Theobromine undergoes enterohepatic recirculation
95
Q

What is the lethal dose for caffeine toxicity?

A

140mg/kg

96
Q

Mothball/moth repellant toxicity

A
  • Contains either naphthalene or paradichlorobenzene
  • Naphthalene causes acute oxidative hemolytic anemia, heinz bodies, occ methemoglobinemia
  • Cats are more sensitive
97
Q

Alfatoxins

A
  • Metabolites produced by Aspergillus & Penicillum fungi that may cause acute hepatic failure
  • Days to weeks of exposure before clinical signs develop
  • Binds and interferes with DNA, RNA, and protein function leading to carcinogenic, teratogenic, mutagenic, and acute hepatotoxic effects
  • May have coumadin like effect that may contribute to hypocoagulable states
98
Q

Tremorgens

A
  • Produced as a result of fungal metabolism
  • Penitrem A & roquefortine
  • Produced by Penicillium, Aspergillus, Clavicepts
  • Excreted in bile and prone to enterohepatic recirculation
  • Lipophilic and crosses BBB –> multiple effects on neurotransmitter release
99
Q

What happens in organophosphate toxicity?

A
  • Insecticides
  • Causes acute irreversible inhibition of acetylcholinesterase activity
  • Acetylcholinesterase is responsible for breaking down acetylcholine. When not broken down effectively, the abundance of acetylcholine can dramatically interfere with autonomic nervous system function
100
Q

What sign is common in organophosphate toxicity that can distinguish it from other tremorgens?

A

Miosis

101
Q

What drug is utilized as a parasympatholytic agent to combat muscarinic signs of organophosphate toxicity?

A

Atropine/muscarinic

102
Q

What drug reactivates the acetychloinesterase that has been inhibited in organophosphate toxicity?

A

Pralioxime/nicotinic

103
Q

What are permethrins?

A

Derived from Chrysantheum cinerariaefolium plant and used for flea/tick control

104
Q

What are pyrethroids?

A

Synthetically derived and are more potent, toxic, and stable

105
Q

Which species is more sensitive to permethrins/pyrethroids?

A

Cats; toxicities ocur crom inadvertent dog dose given to cat. Wide safety margin in dogs

106
Q

What is the MOA of permethrins?

A
  • Bind to membrane lipid phase of nerve cells, slowly opening and closing of neural Na channels, resulting in repetitive nerve firing
  • Less than 1% of Na channels must be affected to produce neuro signs
  • Also act as GABA antagonists
  • More potent on Na channels at lower temps because Na channels of insects work at lower temp
107
Q

Methocarbamol administration should not exceed what dose?

A

> 330mg/kg/day

108
Q

What can be used to treat permethrin toxicity?

A
  • Methocarb more useful than anticonvulsants
  • Dexmedetomidine
  • ILE (lipid soluble)
109
Q

What is the toxic component of rhododendrons/azaleas?

A

Grayanglycocide, a type of diterpinoid compound

110
Q

What is the MOA of rhododendrons?

A
  • Binds to, and produces a modified opening of sodium channels, which delays repolarization of ventricular muscle fibers
  • Toxin present in all parts of plant
111
Q

Are pointsettas toxic?

A

They are a mild GI irritant and therefore self liniting due to vomiting of plant parts

112
Q

What is the cycad plant?

A

Sago palm

113
Q

What parts of the sago palm are toxic?

A

All parts. Highest concentration in seeds

114
Q

What are the 3 toxicants in sago palm?

A
  • Methylazoxymethanol (MAM)
  • Betamethylamino-L- alanine (BMAA, a neurotoxic amino acid)
  • Unidentified toxin
115
Q

What kind of toxicant is sago palm?

A

Hepatic necrosis but can also potentially cause poisoning of the cerebellum

116
Q

What chemistry changes can be seen with sago palm toxicity?

A

Elevated ALT, AST, ALP, TBIL 24-48 hours post ingestion

117
Q

How is sago palm toxicity treated?

A
  • Aggressive decontamination and multiple doses of AC
  • No antidote
118
Q

What is the mortality rate of sago palm toxicity if hepatic necrosis has occurred?

A

75%

119
Q

What is the minimal toxic dose for salt ingestion?

A

As little as 2g/kg

120
Q

Is charcoal effective for salt toxicity?

A

No

121
Q

How does salt toxicity cause CNS signs?

A
  • Na freely passes the BBB into cerebral circulation but requires active transport to return to serum
  • The brain protects itself from hyperosmolar conditions by forming idiogenic osmoles to prevent dehydration of neural cells
  • Lowering serum Na too rapidly will cause cerebral edema as water shifts back into cerebral circulation
122
Q

How quickly can you lower Na?

A
  • No more than 0.5-1mEq/L/hr
  • Max 8-12 mEq/L/24h
123
Q

How does strychnine exert its effect?

A

Antagonises glycine, one of the body’s main inhibitory neurotransmitters and results in CNS excitation

124
Q

What are the toxic doses for strychnine?

A

Dogs: 0.75mg/kg
Cats: 2mg/kg

125
Q

What is the mortality rate for strychnine?

A

60%

126
Q

How do you treat strychnine toxicity?

A
  • Lipophilic: AC, ILE
  • IVFT, anticonvulsants, anesthetics, methocarbamol
  • Ion trapping with IV or PO ammonium chloride may acidify urine and enhance
127
Q

How many doses of AC are needed for thyroid medication toxicities?

A

One

128
Q

Which thyroid medication is most frequently seen in overdose?

A

L-thyroxine

129
Q

When are severe signs of thyroid medication toxicity seen?

A

> 1mg/kg

130
Q

Why is xylitol toxic to dogs?

A
  • It causes insulin release up to 6x greater than equivalent dose of glucose and it is rapidly absorbed in GIT
131
Q

What is a toxic dose for xylitol?

A

As low as 0.1g/kg

132
Q

How quickly can hypoglycemia be seen in xylitol tox?

A

Within 30-60 minutes

133
Q

Why can hypokalemia be seen in xylitol tox?

A

Due to insulin release driving K into cells

134
Q

What does of xylitol is considered to be hepatotoxic?

A

> 0.5g/kg

135
Q

Are dogs still at risk of hepatic necrosis if they don’t present hypoglycemic?

A

Yes

136
Q

Is AC effective in xylitol tox?

A

No

137
Q

What is a poor prognostic indicator for xylitol?

A

Phosphatemia

138
Q

At what dose does zinc toxicity occur?

A

> 100mg/kg

139
Q

What does zinc do to the body?

A
  • Causes severe intravascular hemolysis, GI irritation, renal injury
  • Free zinc is released, which creates zinc salts
  • These salts are potentially caustic to GIT and can have a direct irritant and corrosive effect
  • Zinc salts can lead to RBC oxidative damage
140
Q

What does the rate of zinc release rely on?

A

Gastric pH, presence/absence of ingesta, and length of time in stomach

141
Q

What can zinc do to a Coomb’s test?

A

Cause a positive test in the absence of primary autoimmune disorder

142
Q

What lab changes can be seen in zinc tox?

A
  • Inflammatory leukogram
  • Regenerative anemia
  • Basophilic stippling
  • Spherocytes
  • Heinz bodies
  • Elevated TBIL
  • Elevated LE
  • nRBC
  • Coagulopathy
143
Q

Is AC effective for zinc tox?

A

No

144
Q

Chelation therapy for zinc tox is (recommended/contraindicated/controversial)

A

Controversial

145
Q

What is zinc phosphide?

A

The actige ingredient in mole/gopher powders and rodenticides

146
Q

How does zinc phosphide cause toxicity?

A

In moist and acidic environments (like the stomach), it undergoes a chemical reaction to form toxic phosphine gas - highly toxic
- Inibits oxidative phosphorylation interupting cellular energy and producing processes in mitochondria that result in cell death, peroxidation, and cellular oxidative damage
- Toxicity can progress to neuro signs

147
Q

What is the lethal dose for zinc phosphide?

A

20-40mg/kg in dogs and cats

148
Q

What stomach conditions will exacerbate zinc phosphide tox?

A
  • Recent ingestion of food because food promotes gastric acid secretion, leading to more gas
  • Increasing gastric pH with NaHCO3 will slow hydrolysis into gas
149
Q

What lab changes can be seen in zinc phosphide tox?

A
  • Hypoglycemia
  • Elevated LE
  • Azotemia
  • Metabolic acidemia
150
Q

How do you treat zinc phosphide tox?

A
  • Emesis
  • AC
  • Supportive: IVFT, antiemetics, gastroprotectants, anti-oxidants

VTS (17 decks)

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